Methods: So far, seven patients (f:m 5:2, SAH Â°III-V WFNS, 3 aneurysms coiled, 4 clipped). All patients were monitored for ICP (separate burr hole/external drainage) and CBF (Qflow500, Hemedex), ptiO2 (Licox, Integra), and MD (CMA) through a frontal bolt kit. Episodes of hypoperfusion (rCBF≤18ml/min/100g) and hypoxia (ptiO2<10mmHg) had to last for at least 10 minutes to be counted. Pathological thresholds in MD were defined as glutamate>5ÂµM, lactate>5mM and L/P-ratio>25.

Results: Overall MCM-time was 228Â±81.0 hours. Every patient revealed multiple episodes of cerebral hypoperfusion. 255 such episodes were recognized in all patients but only 11 episodes of cerebral hypoxia. In median (25-;75-quartile), 48.1% (24.6; 92.6%) of the monitored rCBF was below the ischemic threshold and 1.5% (0.6; 17.5%) of the ptiO2 data were hypoxic. In two patients, VSP developed during monitoring and resulted in infarction on control CT. These patients had simultaneous episodes of hypoperfusion and hypoxia for 526 and 1060 minutes and showed pathological MD values. One patient presented with severe VSP on initial angiography. In this patient, perfusion and microdialysis were pathological throughout the monitoring period. In three patients, no simultaneous episodes of hypoperfusion/hypoxia occurred, these patients were not affected by VSP.

Conclusions: The exclusive monitoring of rCBF or ptiO2 may be insufficient to detect relevant ischemia due to VSP alone. Short episodes of hypoperfusion do not necessarily seem to lead to definite tissue damage. However, simultaneous hypoperfusion and hypoxia for several minutes with according pathological metabolic patterns are indicative for developing infarction due to VSP. Thus, the Multimodal Cerebral Monitoring approach seems to be of great value to interpret online assessed data in SAH patients.